Postprandial hyperlipidemia and atherosclerosis.

The development of the remnant like particle (RLP) method for conveniently measuring serum remnant lipoprotein levels in 1993 promoted much research on atherogenic significance and metabolism of remnant lipoproteins. This research brought about many results as the following. A novel apolipoprotein B48 receptor incorporating remnant lipoproteins into macrophages in arterial wall was discovered and the structure of the gene of the receptor was clarified. The expression of apolipoprotein B100 was recognized in the human small intestine, suggesting that dietary very low density lipoproteins (VLDL) might be synthesized in the human small intestine and converted into VLDL remnants and low density lipoproteins (LDL). It is recognized that the atherosclerotic risk of postprandial hyperlipidemia is derived from an increase of remnant lipoproteins and that measurement of serum RLP levels in postprandial state is more sensitive and necessary for evaluating an atherosclerotic risk because serum RLP levels remain high all day in patients with diabetes mellitus or coronary heart disease. The relation between postprandial hyperlipidemia and insulin resistance was clarified.